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Omega-3 reduces Depression. Anxiety, Stress, PTSD, etc. – Aug 2018

Food for Mood: Relevance of Nutritional Omega-3 Fatty Acids for Depression and Anxiety

Front. Physiol., 06 August 2018 | https://doi.org/10.3389/fphys.2018.01047
Thomas Larrieu*† and Sophie Layé*
UMR 1286, NutriNeuro: Laboratoire Nutrition et Neurobiologie Intégrée, Institut National de la Recherche Agronomique, Université de Bordeaux, Bordeaux, France


Vitamin D and Omega-3 category starts with

396 Omega-3 items in category Omega-3 helps with: Autism (8 studies), Depression (29 studies), Cardiovascular (34 studies), Cognition (50 studies), Pregnancy (40 studies), Infant (32 studies), Obesity (13 studies), Mortality (7 studies), Breast Cancer (5 studies), Smoking, Sleep, Stroke, Longevity, Trauma (12 studies), Inflammation (18 studies), Multiple Sclerosis (9 studies), VIRUS (12 studies), etc
CIlck here for details

Items in both categories Omega-3 and Depression:

Anxiety studies include

14+ VitaminDWiki pages with ANXIETY in title
This list is automatically updated

Items found: 15
Title Modified
International Adolescent Anxiety and suicide rates - GBD April 2024 07 Apr, 2024
Half as much anxiety and sleep problems if get lots of vitamin D from food (excluded getting D from supplements) – Feb 2024 23 Feb, 2024
Anxiety, Vitamin D, Omega-3 - many studies 23 Feb, 2024
Low Vitamin D is associated with risk of Depression 5X, Stress 4.8 X, and Anxiety 3.9 X (Saudi Arabia college students) – July 2023 29 Jul, 2023
Parkinson’s – Vitamin D, bone density, insomnia, falls, poor sleep, anxiety – March 2019 10 May, 2023
Anxiety and Depression decreased in senior prediabetics with weekly 25,000 IU of Vitamin D – RCT Sept 2022 22 Dec, 2022
Depression and Anxiety treatment with Vitamin D - probable molecular pathways - June 2022 21 Dec, 2022
Coronary Artery Disease Chest Pain, Anxiety, and Fatigue associated with low vitamin D – Oct 2022 07 Oct, 2022
Anxiety, depression, and suicide have recently surged (Note: Vitamin D, Omega-3, and Magnesium help) – May 2022 29 May, 2022
General Anxiety Disorder treated by weekly Vitamin D (50,000 IU -Omega-3, Mg also help) – Sept 2019 09 Dec, 2019
Omega-3 reduces Depression. Anxiety, Stress, PTSD, etc. – Aug 2018 02 Sep, 2019
Happy Nurses Project gave Omega-3 for 3 months – reduced depression, insomnia, anxiety, etc for a year – RCT July 2018 10 Nov, 2018
Anxiety severity reduced if more than 2 grams of Omega-3 – meta-analysis Sept 2018 19 Sep, 2018
Why is teen anxiety increasing so much (no mention of Magnesium, Vitamin D nor Omega-3) – Oct 2017 11 Oct, 2017
Salmon intervention (vitamin D and Omega-3) improved heart rate variability and reduced anxiety – Nov 2014 11 Feb, 2015

 Download the PDF from VitaminDWiki

The central nervous system (CNS) has the highest concentration of lipids in the organism after adipose tissue. Among these lipids, the brain is particularly enriched with polyunsaturated fatty acids (PUFAs) represented by the omega-6 (ω6) and omega-3 (ω3) series. These PUFAs include arachidonic acid (AA) and docosahexaenoic acid (DHA), respectively. PUFAs have received substantial attention as being relevant to many brain diseases, including anxiety and depression. This review addresses an important question in the area of nutritional neuroscience regarding the importance of ω3 PUFAs in the prevention and/or treatment of neuropsychiatric diseases, mainly depression and anxiety. In particular, it focuses on clinical and experimental data linking dietary intake of ω3 PUFAs and depression or anxiety. In particular, we will discuss recent experimental data highlighting how ω3 PUFAs can modulate neurobiological processes involved in the pathophysiology of anxiety and depression. Potential mechanisms involved in the neuroprotective and corrective activity of ω3 PUFAs in the brain are discussed, in particular the sensing activity of free fatty acid receptors and the activity of the PUFAs-derived endocannabinoid system and the hypothalamic–pituitary–adrenal axis.

Since the discovery of omega-3 (ω3) PUFAs in 1929 by George Burr and Mildred Burr (Burr and Burr, 1929; Spector and Kim, 2015), research on ω3 PUFAs became an appealing topic ranging from their role in cardiovascular risk to more recently neuropsychiatric pathologies such as depression and anxiety, cognitive decline or neurodegenerative diseases (Bazinet and Layé, 2014; Joffre et al., 2014; Coulombe et al., 2017). The relevance of lipids in brain function is illustrated by the fact that the CNS has the highest concentration of lipids in the organism after the adipose tissue (50–60% of the dry weight of the brain; Sastry, 1985). Among these lipids, the brain is particularly greedy for PUFAs from the ω6 and ω3 PUFAs families, in particular the LC PUFA (AA, 20:4n-6) and (DHA, 22:6n-3), respectively (Sastry, 1985). In the Human brain, DHA accounts for 10 to 15% of the total fatty acids (saturated, monounsaturated and PUFAs) in both males and females (McNamara et al., 2007, 2008b). This makes PUFAs indispensable to the normal development and function of the CNS (Makrides and Gibson, 2000; Innis, 2007; Bazinet and Layé, 2014). One hypothesis explaining this abundance in brain tissue is that Homo sapiens in Paleolithic settled around the lakes and seas where access to foods rich in ω3 PUFAs is easy (Bradbury, 2011). It is generally considered that humans evolved on a diet with a ratio of ω6 to ω3 PUFAs equal approximately to 1. During the industrial era, the rapid expansion of Western countries has been associated with drastic changes in the ω6/ω3 PUFAs content of the diet. This is reflected in large quantities of ω6 PUFA-containing foods and smaller amounts of ω3 PUFA-rich foods leading to Western diet being typically poor in ω3 PUFAs. In addition, the intake of saturated fats from lard and butter has been replaced by plant-based PUFAs based on recommendations from health agencies (Gibson et al., 2011). As a result, the use of oils such as sunflower oil which are mostly high in (LA, the precursor of AA) and low in a-linolenic acid (ALA, the precursor of DHA) leads to a marked increase in LA intake. In mammals, LA and ALA cannot be synthesized de novo and need to be provided through the diet (Simopoulos, 1991; Gibson and Makrides, 2001). These essential PUFAs are metabolized into LC PUFAs using the same enzymatic pathway, meaning that LA and ALA are in competition for endogenous conversion to their respective LC forms AA, and DHA (Figure 1) but also for their entry into the brain (Bazinet and Layé, 2014). Of importance, ALA bioconversion into DHA through several cycles of elongation (ELOVLs) and desaturation (Δ5 and Δ6 desaturases) is in the range of 0.05% (Burdge et al., 2003) to 4% (Emken et al., 1994) and might not be sufficient to cover brain needs. This led to the recommendation of dietary intake of oily fish rich in the LC ω3 PUFAs DHA and EPA (Tejera et al., 2016). Overall, western diets which are rich in LA (coming from vegetable oils rich in LA) and poor in ALA and DHA (coming from fat fish, sea food or certain algae) have created “a conditional essentiality for ω3 PUFAs” as previously described by Cunnane (2003) and Gibson et al. (2011). Indeed, the amount of LC ω3 PUFAs needed to compensate this lack in western diet is likely to increase, which is not sustainable in the actual context of fish stock decline (Fernandes and Cook, 2013). . . .

Created by admin. Last Modification: Monday December 9, 2019 12:35:54 GMT-0000 by admin. (Version 4)

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